Role of the Cardiologist in Management of Subarachnoid Haemorrhage

2002 ◽  
Vol 15 (5) ◽  
pp. 625-633 ◽  
Author(s):  
F. Gaita ◽  
L. Formato ◽  
F. Bianchi ◽  
L. Vivalda ◽  
C. Giustetto ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Subarachnoid Haemorrhage ◽  
Pulmonary Oedema ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Aneurysmal Subarachnoid Haemorrhage ◽  
Ecg Changes ◽  
St Segment ◽  
Ecg Abnormalities

Patients with aneurysmal subarachnoid haemorrhage (SAH) frequently have cardiovascular complications that include: blood pressure fluctuations, cardiac arrhythmias and ECG changes. ECG abnormalities, haemodynamic instability and pulmonary oedema, frequently associated with this pathologic condition, contribute to the morbidity and mortality of subarachnoid haemorrhage (SAH). Actually ECG changes occur in 50% to 100% of the patients during the acute stage of SAH, with the most common abnormalities involving the ST segment, T wave and QT interval. In most cases, these abnormalities are clinically inconsequential and are attributed to neurally mediated electrophysiological effects. Some SAH patients, however, show evidence of structural cardiac damage. ECG abnormalities which are indistinguishable from those due to acute myocardial infarction (ST segment elevation or depression) have occasionally been reported in SAH. These patients exhibited findings (which are completely reversible) similar to an acute myocardial infarction on ECG examination, as well as elevated cardiac enzymes and findings of left ventricular wall motion abnormalities, mostly anterior wall akynesis, causing the reduction of left ventricular ejection fraction. Occurrence of pulmonary oedema has been described in ten to 25% of SAH patients. Pulmonary oedema may be neurogenic or cardiogenic in origin and both are a consequence of increased adrenergic tone. There is evidence that the most important consequence of cardiovascular effects secondary to subarachnoid haemorrhage is increased susceptibility to sudden death. The increased adrenergic tone, due to high catecholamine levels and sympathetic cranial nerves stimulation can explain the origin of tachyarrhythmias. The mechanism proposed to explain the origin of bradyarrhythmias is an increased vagal tone.

Abstract 13194: The Effects of Methotrexate Therapy on Myocardial Infarction With ST-Segment Elevation (TETHYS Trial)

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Daniel M Moreira ◽  
Roberto L da Silva ◽  
Maria E Lueneberg ◽  
Tammuz Fattah ◽  
Carlos A Gottschall
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Troponin I ◽  
Experimental Studies ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
St Segment Elevation ◽  
Timi Frame Count ◽  
St Segment

Introduction: Acute myocardial infarction provokes inflammatory activation. Methotrexate is one drug that has been shown to have anti-ischemic effects in experimental studies. Hypothesis: Methotrexate could reduce inflammation and the ischemia area in acute myocardial infarction Methods: We randomly assigned patients with myocardial infarction with ST-segment elevation to receive either methotrexate (0.05 mg/kg bolus followed by 0.05 mg/kg/h for 6 h) or matching placebo (riboflavin sodium phosphate 0.1%, in order to preserve double-blinding) at a ratio of 1:1. Patients in both groups were given a 5mg single dose of folic acid. The primary endpoint was infarct size, determined by the area under the curve (AUC) for creatine kinase (CK) release. Secondary endpoints were AUC of CK-MB and AUC of troponin I; peak CK, peak CK-MB and troponin I; B-type natriuretic peptide (BNP) level, high-sensitivity C-reactive protein (hsCRP) result and erythrocyte sedimentation rate (ESR); left ventricular ejection fraction (LVEF); TIMI frame count; Killip score; mortality and reinfarction incidence. The safety endpoint was the incidence of adverse reactions. Results: We included 84 patients. The AUC of CK was 78,861.00 in the methotrexate group and 68,088.00 in the placebo group (P=0.10). Patients given methotrexate and placebo exhibited, respectively, AUC for CK-MB of 9,803.40 and 8,037.00 (P=0.42); AUC for troponin I of 3,691.11 and 2,132.63 (P=0.09); peak CK of 2,806.00 and 2,147.00 (P=0.05), peak CK-MB of 516.00 and 462.25 (P=0.25) and peak troponin I of 121.00 and 85.05 (P=0,06). At 3 months, LVEF was lower in patients who received methotrexate (48.97±14.09%) than in patients given placebo (56.37±9.97%) (P=0.01). There were no differences in hsCRP, ESR, BNP, Killip scores or TIMI frame count. There were also no differences in reinfarction or mortality rates or in incidence of side effects, with the exception of higher median serum glutamic-pyruvic transaminase (SGPT) levels in the methotrexate group. Conclusions: Methotrexate did not reduce infarction size and worsened LVEF at 3 months.

Randomized, double blind, placebo-controlled, safety and efficacy study of dutogliptin in combination with filgrastim in early recovery post-MI: rationale, design and first interim analysis

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
D Von Lewinski ◽  
B Merkely ◽  
I Buysschaert ◽  
R.A Schatz ◽  
G.G Nagy ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Stem Cells ◽  
Adverse Events ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Funding Source ◽  
Early Recovery ◽  
Ventricular Ejection Fraction ◽  
Combined Application

Abstract Background Regenerative therapies offer new approaches to improve cardiac function after acute ST-elevation myocardial infarction (STEMI). Mobilization of stem cells and homing within the infarcted area have been identified as the key mechanisms for successful treatment. Application of granulocyte-colony stimulating factor (G-CSF) is the least invasive way to mobilize stem cells while DDP4-inhibitor facilitates homing via stromal cell-derived factor 1 alpha (SDF-1α). Dutogliptin, a novel DPP4 inhibitor, combined with stem cell mobilization using G-CSF significantly improved survival and reduced infarct size in a murine model. Purpose We initiated a phase II, multicenter, randomized, placebo-controlled efficacy and safety study (N=140) analyzing the effect of combined application of G-CSF and dutogliptin, a small molecule DPP-IV-inhibitor for subcutaneous use after acute myocardial infarction. Methods The primary objective of the study is to evaluate the safety and tolerability of dutogliptin (14 days) in combination with filgrastim (5 days) in patients with STEMI (EF <45%) following percutaneous coronary intervention (PCI). Preliminary efficacy will be analyzed using cardiac magnetic resonance imaging (cMRI) to detect >3.8% improvement in left ventricular ejection fraction (LV-EF). 140 subjects will be randomized to filgrastim plus dutogliptin or matching placebos. Results Baseline characteristics of the first 26 patients randomized (24 treated) in this trial reveal a majority of male patients (70.8%) and a medium age of 58.4 years (37 to 84). During the 2-week active treatment period, 35 adverse events occurred in 13 patients, with 4 rated as serious (hospitalization due to pneumonia N=3, hospitalization due to acute myocardial infarction N=1), and 1 adverse event was rated as severe (fatal pneumonia), 9 moderate, and 25 as mild. 6 adverse events were considered possibly related to the study medication, including cases of increased hepatic enzymes (N=3), nausea (N=1), subcutaneous node/suffusion (N=1) and syncope (N=1). Conclusions Our data demonstrate that the combined application of dutogliptin and G-CSF appears to be safe on the short term and feasible after acute myocardial infarction and may represent a new therapeutic option in future. Funding Acknowledgement Type of funding source: Other. Main funding source(s): This research is funded by the sponsor RECARDIO, Inc., 1 Market Street San Francisco, CA 94150, USA. RECARDIO Inc. is funding the complete study. The Scientific Board of RECARDIO designed the study. Data Collection is at the participating sites. Interpretation of the data by the Scientific Board and Manuscript written by the authors and approved by the Sponsor

scholarly journals Electrical storm reveals worse prognosis compared to myocardial infarction complicated by ventricular tachyarrhythmias in ICD recipients

2021 ◽  
Author(s):  
Julian Müller ◽  
Michael Behnes ◽  
Tobias Schupp ◽  
Dominik Ellguth ◽  
Gabriel Taton ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Electrical Storm ◽  
Ventricular Tachyarrhythmias ◽  
Ventricular Ejection Fraction ◽  
St Segment ◽  
All Cause Mortality ◽  
Worse Prognosis

AbstractBoth acute myocardial infarction complicated by ventricular tachyarrhythmias (AMI–VTA) and electrical storm (ES) represent life-threatening clinical conditions. However, a direct comparison of both sub-groups regarding prognostic endpoints has never been investigated. All consecutive implantable cardioverter-defibrillator (ICD) recipients were included retrospectively from 2002 to 2016. Patients with ES apart from AMI (ES) were compared to patients with AMI accompanied by ventricular tachyarrhythmias (AMI–VTA). The primary endpoint was all-cause mortality at 3 years, secondary endpoints were in-hospital mortality, rehospitalization rates and major adverse cardiac event (MACE) at 3 years. A total of 198 consecutive ICD recipients were included (AMI–VTA: 56%; ST-segment elevation myocardial infarction (STEMI): 22%; non-ST-segment myocardial infarction (NSTEMI) 78%; ES: 44%). ES patients were older and had higher rates of severely reduced left ventricular ejection fraction (LVEF) < 35%. ES was associated with increased all-cause mortality at 3 years (37% vs. 19%; p = 0.001; hazard ratio [HR] = 2.242; 95% CI 2.291–3.894; p = 0.004) and with increased risk of first cardiac rehospitalization (44% vs. 12%; p = 0.001; HR = 4.694; 95% CI 2.498–8.823; p = 0.001). This worse prognosis of ES compared to AMI–VTA was still evident after multivariable adjustment (long-term all-cause mortality: HR = 2.504; 95% CI 1.093–5.739; p = 0.030; first cardiac rehospitalization: HR = 2.887; 95% CI 1.240–6.720; p = 0.014). In contrast, the rates of MACE (40% vs. 32%; p = 0.326) were comparable in both groups. At long-term follow-up of 3 years, ES was associated with higher rates of all-cause mortality and rehospitalization compared to patients with AMI–VTA.

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